Background Adults with congenital heart disease (CHD) have been considered potentially high risk for novel coronavirus disease-19 (COVID-19) mortality or other complications. Objectives This study sought to define the impact of COVID-19 in adults with CHD and to identify risk factors associated with adverse outcomes. Methods Adults (age 18 years or older) with CHD and with confirmed or clinically suspected COVID-19 were included from CHD centers worldwide. Data collection included anatomic diagnosis and subsequent interventions, comorbidities, medications, echocardiographic findings, presenting symptoms, course of illness, and outcomes. Predictors of death or severe infection were determined. Results From 58 adult CHD centers, the study included 1,044 infected patients (age: 35.1 ± 13.0 years; range 18 to 86 years; 51% women), 87% of whom had laboratory-confirmed coronavirus infection. The cohort included 118 (11%) patients with single ventricle and/or Fontan physiology, 87 (8%) patients with cyanosis, and 73 (7%) patients with pulmonary hypertension. There were 24 COVID-related deaths (case/fatality: 2.3%; 95% confidence interval: 1.4% to 3.2%). Factors associated with death included male sex, diabetes, cyanosis, pulmonary hypertension, renal insufficiency, and previous hospital admission for heart failure. Worse physiological stage was associated with mortality (p = 0.001), whereas anatomic complexity or defect group were not. Conclusions COVID-19 mortality in adults with CHD is commensurate with the general population. The most vulnerable patients are those with worse physiological stage, such as cyanosis and pulmonary hypertension, whereas anatomic complexity does not appear to predict infection severity.
Objectives To define whether adults with a Fontan circulation, who have life-long venous congestion and limited cardiac output, have impaired glomerular filtration rate (GFR) or elevated urinary biomarkers of kidney injury. Methods We measured circulating cystatin C and creatinine (n=70) and urinary creatinine, albumin, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL) and N-acetyl glucosaminidase (NAG)(n=59) in ambulatory adult Fontan patients and 20 age- and sex- matched controls. Urinary biomarkers were normalized to urine creatinine concentration. Survival free from non-elective cardiovascular hospitalization was compared, by estimated GFR and urinary biomarker levels using survival analysis. Results Cystatin C GFR was lower in the Fontan group compared with controls (114.2±22.8 vs. 136.3±12.8mL/min/1.73m2, p<0.0001); GFR<90mL/min/1.73m2 in 14.3% vs. 0% of controls. Albumin-to-creatinine ratio (ACR), KIM-1 and NAG were elevated compared with controls; ACR=23.2 [7.6–38.3] vs. 3.6 [2.5–5.7]mg/g, p<0.0001; NAG=1.8 [1.1–2.6] vs. 1.1 [0.9–1.6]U/g, p=0.02; KIM-1=0.91 [0.52–1.45] vs. 0.33 [0.24–0.74]ng/mg, p=0.001. Microalbuminuria, ACR>30mg/g, was present in 33.9% of the Fontan patients but in none of the controls. Over median 707 [IQR 371–942] day follow-up, 31.4% of patients had a clinical event. Higher KIM-1 and NAG were associated with higher risk of non-elective hospitalization or death (HR/+1SD=2.1, 95%CI=1.3–3.3, p=0.002; HR/+1SD=1.6, 95%CI=1.05–2.4, p=0.03, respectively); cystatin C GFR was associated with risk of the outcome (HR/+1SD=0.66, 95%CI=0.48–0.90, p=0.009) but creatinine-based GFR was not (HR/+1SD=0.91, 95%CI=0.61–1.38, p=0.66). Neither ACR nor NGAL were associated with events. Conclusions The Fontan circulation is commonly associated with reduced estimated GFR and evidence for glomerular and tubular injury. Those with lower cystatin C GFR and tubular injury are at increased risk of adverse outcomes.
BackgroundGalectin‐3 may play a role in cardiac and noncardiac fibrosis, and elevated circulating levels of this protein predict adverse outcomes in patients with heart failure who do not have congenital heart disease. We investigated galectin‐3 in adults with single‐ventricle Fontan circulation, patients who are prone to premature clinical deterioration in the context of extensive multiorgan fibrosis.Methods and ResultsWe measured plasma galectin‐3 concentrations in 70 ambulatory adult Fontan patients and 21 age‐ and sex‐matched control participants. Galectin‐3 level was significantly higher in the Fontan group (11.85 ng/mL, interquartile range 9.9 to 15.0 ng/mL) versus the control group (9.4 ng/mL, interquartile range 8.2 to 10.8 ng/mL; P<0.001). Among Fontan patients, galectin‐3 was positively correlated with age, uric acid, and high‐sensitivity C‐reactive protein and negatively correlated with estimated glomerular filtration rate. There was no significant relationship between galectin‐3 and oxygen saturation, Fontan type, or ventricular morphology. Over a median follow‐up of 461 days, 15 events occurred among the Fontan patients: 12 nonelective hospitalizations (with 2 subsequent deaths) and 3 deaths without prior hospitalization. Patients with elevated galectin‐3 (n=19, defined as >2 SD above the control group mean value) had a higher risk of nonelective hospitalization or death (hazard ratio 6.0, 95% CI 2.1 to 16.8, P<0.001). This relationship persisted after individual adjustment for covariates including age, New York Heart Association functional class, C‐reactive protein, and estimated glomerular filtration rate and after multivariable adjustment for independently predictive covariates (hazard ratio 9.2, 95% CI 2.4 to 35.2, P=0.001).ConclusionsGalectin‐3 concentrations are elevated among adults with a Fontan circulation, and elevated galectin‐3 is associated with an increased risk of nonelective cardiovascular hospitalization or death.
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